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91.
Annie B. Elliott 《Cellular and molecular life sciences : CMLS》1968,24(6):557-558
Résumé En employant des crapauds pour doser l'action des peptides sur la perméabilité de la peau, l'effet hydrosmotique de l'arginine8-vasotocine s'est montré 200 fois plus puissant que celui de l'ornithine8-oxytocine. Ce fait confirme l'importance hydrosmotique de l'acide aminé arginine dans la position 8. Tous 2 ont eu un effet natriférique, mais ce ne fut pas le cas de la lysine8-vasopressine et l'ornithine8-vasopressine. L'importance natriférique de l'acide aminé isoleucine dans la position 3 en est confirmée. 相似文献
92.
The first published observations on the nesting and predatory behavior of Tachysphex antennatus Fox, T. occidentalis Pulawski, T. williamsi Bohart, T. yolo Pulawski, T. alpestris Rohwer, T. clarconis Viereck, T. apricus Pulawski, and T. cockerellae Rohwer are presented herein. Also included are host and behavioral data on T. tarsatus (Say), T. apicalis fusus Fox, T. similis Rohwer, T. ashmeadii Fox, and T. mundus exsectus Fox. 相似文献
93.
Peptide-induced conformational change of the class I heavy chain 总被引:12,自引:0,他引:12
There is evidence that peptide ligands take part in the assembly of class I molecules. In particular, addition of peptides to extracts of the mutant cells RMA-S and .174/T2, in which stable assembly of class I does not occur, results in a conformational change in the class I heavy chain and stable association of the heavy chain with beta 2-microglobulin (beta 2m). Thus specific peptides may stabilize or induce a conformational change in the class I heavy chain that results in a rise in the binding affinity of the heavy chain for beta 2m (Fig. 1a). Here we show that peptides have two cooperative roles in class I assembly. Specific short peptides (9-10 amino acids) can induce folding of the heavy chain in the absence of beta 2m. Both short (nine amino acids) and longer sequences (15 amino acids) can stabilize performed low-affinity complexes of heavy chain and beta 2m. To alter the conformation of free heavy chains, the peptides must be exactly the correct size, and they are found to correspond to the sequences isolated from infected cells. This property may therefore be the basis for selection of epitopes presented in vivo. 相似文献
94.
Calmodulin interacts with MLO protein to regulate defence against mildew in barley 总被引:29,自引:0,他引:29
Kim MC Panstruga R Elliott C Müller J Devoto A Yoon HW Park HC Cho MJ Schulze-Lefert P 《Nature》2002,416(6879):447-451
In plants, defence against specific isolates of a pathogen can be triggered by the presence of a corresponding race-specific resistance gene, whereas resistance of a more broad-spectrum nature can result from recessive, presumably loss-of-regulatory-function, mutations. An example of the latter are mlo mutations in barley, which have been successful in agriculture for the control of powdery mildew fungus (Blumeria graminis f. sp. hordei; Bgh). MLO protein resides in the plasma membrane, has seven transmembrane domains, and is the prototype of a sequence-diversified family unique to plants, reminiscent of the seven-transmembrane receptors in fungi and animals. In animals, these are known as G-protein-coupled receptors and exist in three main families, lacking sequence similarity, that are thought to be an example of molecular convergence. MLO seems to function independently of heterotrimeric G proteins. We have identified a domain in MLO that mediates a Ca2+-dependent interaction with calmodulin in vitro. Loss of calmodulin binding halves the ability of MLO to negatively regulate defence against powdery mildew in vivo. We propose a sensor role for MLO in the modulation of defence reactions. 相似文献
95.
The correct repair of double-strand breaks (DSBs) is essential for the genomic integrity of a cell, as inappropriate repair
can lead to chromosomal rearrangements such as translocations. In many hematologic cancers and sarcomas, translocations are
the etiological factor in tumorigenesis, resulting in either the deregulation of a proto-oncogene or the expression of a fusion
protein with transforming properties. Mammalian cells are able to repair DSBs by pathways involving homologous recombination
and nonhomologous end-joining. The analysis of translocation breakpoints in a number of cancers and the development of model
translocation systems are beginning to shed light on specific DSB repair pathway(s) responsible for the improper repair of
broken chromosomes.
Received 19 June 2001; received after revision 6 September 2001; accepted 11 September 2001 相似文献
96.
Gilman AG Simon MI Bourne HR Harris BA Long R Ross EM Stull JT Taussig R Bourne HR Arkin AP Cobb MH Cyster JG Devreotes PN Ferrell JE Fruman D Gold M Weiss A Stull JT Berridge MJ Cantley LC Catterall WA Coughlin SR Olson EN Smith TF Brugge JS Botstein D Dixon JE Hunter T Lefkowitz RJ Pawson AJ Sternberg PW Varmus H Subramaniam S Sinkovits RS Li J Mock D Ning Y Saunders B Sternweis PC Hilgemann D Scheuermann RH DeCamp D Hsueh R Lin KM Ni Y Seaman WE Simpson PC O'Connell TD Roach T Simon MI 《Nature》2002,420(6916):703-706
The Alliance for Cellular Signaling is a large-scale collaboration designed to answer global questions about signalling networks. Pathways will be studied intensively in two cells--B lymphocytes (the cells of the immune system) and cardiac myocytes--to facilitate quantitative modelling. One goal is to catalyse complementary research in individual laboratories; to facilitate this, all alliance data are freely available for use by the entire research community. 相似文献
97.
R J Elliott 《Nature》1965,206(981):315-317
98.
99.
Organization of actin in a mammalian smooth muscle 总被引:3,自引:0,他引:3
100.